Mammalian response to injury or inflammation is a complex series of events. Shortly after an event which elicits an inflammatory cascade, the release of eicosanoids is initiated. The release of eicosanoids is mediated by the activation of Phospholipase A.sub.2 (PLA.sub.2) which releases arachidonic acid from phospholipids. Arachidonic acid is subsequently converted into the biologically active compounds known as eicosanoids. Prostaglandins, prostacyclines, leukotrienes and thromboxanes are all examples of eicosanoids. This series of events is often described as the arachidonic acid cascade.
Recently, a correlation has been shown between increased levels of phospholipase A.sub.2 activating protein (PLAP) in vivo and rheumatoid arthritis. Research concerning PLAP and other initiators of the arachidonic acid cascade has recently shown that PLAP stimulates neutrophil aggregation and chemokinesis (Bomalaski et al., J. Immuno. 11:3957-3962 (1989)).